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- Title
Nicorandil prevents epinephrine-induced arrhythmias in halothane-anesthetized rats by nitric oxide-dependent mechanism.
- Authors
Kawai, Yusuke; Hayashi, Yukio; Ito, Isao; Kamibayashi, Takahiko; Takada, Koji; Kagawa, Kiyokazu; Yamatodani, Atsushi; Mashimo, Takashi
- Abstract
The effect of opening ATP-sensitive K+ channels on the genesis of arrhythmias is still controversial. We investigated the effect of nicorandil, an ATP-sensitive K+ channel opener, on the genesis of halothane-epinephrine arrhythmias in rats. We also clarified the involvement of nitric oxide in the effect of nicorandil. Furthermore, we studied the effect of levcromakalim, another ATP-sensitive K+ channel opener, for comparison. Nicorandil and levcromakalim significantly increased the arrhythmogenic thresholds of epinephrine in a dose-dependent manner. On the other hand, nitroprusside, a potent vasodilator (5.0 µg/kg per min), did not exert antiarrhythmic action significantly. Both glibenclamide (non-specific ATP-sensitive K+ channel blocker) and 5-hydroxydecanoate (mitochondrial ATP-sensitive K+ channel blocker) inhibited the antiarrhythmic action of nicorandil. Although pretreatment with N-ω-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, did not modulate the genesis of halothane-epinephrine arrhythmias in the absence of nicorandil, it completely abolished the antiarrhythmic action of nicorandil, but not the effect of levcromakalim. We concluded that nicorandil dose-dependently inhibited halothane-epinephrine arrhythmias through mitochondrial ATP-sensitive K+ channels and nitric oxide is required for the antiarrhythmic effect of nicorandil.
- Subjects
ARRHYTHMIA; NITRIC oxide; ADRENALINE; ANESTHETICS; HYPOGLYCEMIC agents; DRUGS; PHARMACOLOGY
- Publication
Naunyn-Schmiedeberg's Archives of Pharmacology, 2002, Vol 366, Issue 6, p522
- ISSN
0028-1298
- Publication type
Article
- DOI
10.1007/s00210-002-0644-9